Addiction Treatment Blog

In 1954, Olds and Milner discovered that there appeared to be pleasure spots in the brain. Implanting electrodes in certain areas of the brain, through which a rat can give itself an electric current by pressing on a lever, produced in most brain areas nothing of note. In some areas, however, the rats seemed keen on the effects of self-stimulation and, in some cases, if left to their own devices would self-stimulate to the exclusion of all else – even food and drink.

As mentioned, noradrenaline was discovered in the brain in 1954. In 1959, a second catecolamine, dopamine, was identified, which was shown to be deficient in Parkinson’s disease.

The later mapping of dopamine-containing neurones has shown that they too, like noradrenergic neurones, tend to originate in a discrete area, the ventral tegmentum. Some of these neurones run to strictly motor areas of the brain and constitute the nigrostriatal system, and it is loss of nerve calls in this pathway that leads to Parkinson’s disease. Read more…

If the induction of appetites and cravings, which has been hitherto seen as psychological dependence, is not in fact any more psychological than the physical dependence that underlies withdrawal, is there any other psychology involved? There almost certainly is (1). For example LSD, phencyclidine and many of the new designer drugs do not cause either type 1 or 2 physical dependence. Yet they are increasingly abused, despite evidence that many of these compounds may be fatal. Phencyclidine, for example, has led to a considerable number of fatalities and, despite not leading to any obvious euphoria, during the 1980s became for a period the second most common drug of abuse in the USA. Why?

Common to many of these drugs is the fact that they alter consciousness and, as a result, are interesting to take. On tis basis, one explanation that may account psychedelics, opiates or alcohol, there is a certain amount of playful activity. Read more…

Over the past two decades there appears to have been a shift within health care from an expectation that patients with medical problems should entrust themselves passively to the care of physicians to an expectation that they should co-operate in their own care and indeed have some responsibility for the outcome of medical procedures they undergo. The changes are reflected in the terms we used; the word patient, which means someone who endures, is being replaced by terms such as client or consumer, which suggest a more active and discriminating participant in the medical process.

Nowhere is this shift more clear than when it comes to the question of what is known as informed consent. Informed consent was not an issue in medical practice 20 years ago. Today it forms a central issue in a number of ethical codes from the Nuremberg Code to the Helsinki Code as well as Codes originating from the Food and Drugs Administration (FDA) in the United States and the US Department of Health. Read more…

Effects of Drugs on Sex

Table of Contents

• Potency
• Orgasm
• Libido
• Aphrodisiacs
• Yohimbine
• Trazodone
• Nefazodone and Cyproheptadine
• Glyceril Trinitrate
• Transcutaneous Absorption
• Intracaversonal Injections
• Bethanecol
• Dyspareunia and Orgasm
• Libido
• Anaphrodisiacs
• Sex Addiction Treatment Clinic
• Do You Need Help?

Read more…

Barbiturates

Concerns about the over-prescription of benzodiazepines in recent years have led some prescribers to look at alternative hypnotic agents – either older compounds such as members of the barbiturate or chloral families, antidepressants, or neuroleptics with a sedative profile. There are a number of problems with such prescriptions as will become clear.

Chloral Compounds

Chloral compounds (see the table below) were first produced in 1869. Their sedative effects were quickly recognised, leading to their use as hypnotics among other things. A number of factors militated against their widespread use. One was the difficulty in making them in other than foul tasting liquid formats. The subsequent discovery of the barbiturates, just before the First World War, largely put paid to them. Before that, however, many patients admitted to mental hospitals were treated with chloral draughts and would appear to have done well. Read more…

Benzodiazepine Structure

What is the place for hypnotics in this scheme of things? Basically the same place that alcohol has occupied for centuries. Most of us every so often, if we are anxious, worked up or have a lot of things on our mind will have on occasion resorted to alcohol to knock ourselves out. This it doers effectively on an episodic basis. There are drawbacks to alcohol, however. One is that it may produce a rebound insomnia – it knocks you out but also wakes you up several hours later as the effects wear off. It may also wake you up to pass urine or because of dehydration.

Hypnotics do roughly the same thing, with similar benefits and side effects. Judiciously used, they are wonderful. Taken in the early stages of a problem they may abort the later development of habitual anxiety-based insomnia. Taken too regularly or chronically, they may produce their own problems.

The place for the hypnotics lies in the management of sleeplessness rather than in the management of insomnia. Where there is genuine sleeplessness stemming from jet lag or an underlying physical condition, or problems with falling asleep in what may be uncomfortable circumstances or situations of stress, a hypnotic may be of great benefit. The presumption in these cases is that there is a transient sleeplessness and the condition is being managed until normality returns. In certain circumstances, such as where a chronic physical condition regularly compromises sleep, it would seem that hypnotics can be used chronically without causing much in the lines of dependence or other problems. Under the side effects section below, problems such as the risks posed to driving from sedative effects of these drugs will be outlined but it should also be borne in mind that the fatigue consequent on sleeplessness is seen as a rather trivial issue. Read more…

Lithium Pellets

There are some suggestions from as early as the 2nd century AD that spring waters that were alkaline (which would be expected with a high concentration of lithium salts) were known to be of some use in the treatment of overactive states such as mania (1).

Lithium itself was isolated first by August Arfwedson in 1817. It was named lithium as it was found in stone – lithos being the Greek for stone. During the 1850s alkaline compounds, like lithium, were known to be of some use in preventing gout by interfering with the precipitation of uric acid in the blood and joints. At the time mania and melancholia were often seen as being part of the same family of diseases as gout and this led to the use of lithium for these conditions also. As early as 1880, the use of lithium in this manner led Carl Lange to suggest that it might have a role in preventing episodes of periodic depression.

Surprisingly, however, despite these discoveries and what would now appear to be correct hunches, lithium slipped out of use for mood disorders and had to be rediscovered in 1949. In part this was because of its side effects. In the middle of the 19th century, several investigators took lithium and noted that it caused increased urine flow, tremor of the hands and difficulties with memory or concentration, which led to wariness regarding its use. Later in the 1930s, it was used as part of a salt restriction diet in the United States and in many cases it caused such clear cut toxicity that its use was banned by the Foods and Drugs Administration (FDA). Read more…

There are seven major physical treatments for depression at present.

• Tricyclic Antidepressants (Table 1). These have until recently been by far the most widely used.
• The Monoamine Oxidase Inhibitors (MAOIs) (Table 2).
• Reversible Inhibitors of Monoamine Oxidase (RIMAs) (Table 3).
• 5-HT Reuptake Inhibitors (Table 4).
• Other Antidepressants (Table 5).
• Treatments for Bipolar Disorders or Prophylaxis of Recurrent Disorders (Table 6).
• Others (Table 7)

In the last category, a number of other treatments are marketed for or used for depression and they often work, but whether they are antidepressants in the same sense as electroconvulsive therapy (ECT), imipramine or phenelzine is a matter of dispute. The 5-HT-1a agonist, buspirone, has in addition been marketed as an antidepressant, and a further compound from this group, flesinoxan, looks as though it may also emerge as an antidepressant.

Finally, there is also ECT, the mechanism of action of which, and its use clinically will not be discussed at any length in this article. Its role when antidepressants fail to work and in cases of mania will be considered at a later stage. Read more…

Schizophrenia can be dangerous to yourself and others around you if treated incorrectly.

In any consideration of the dopamine hypothesis of schizophrenia, one of the arguments invariably put forward is that psychostimulant drugs, in particular the amphetamines, lead to a mental disorder characterised by prominent paranoid feelings, or outright paranoid delusions. This many authorities have suggested, is a state that is very similar to some schizophrenic states. As the psychostimulants increase brain dopamine levels or neurotransmission, schizophrenia must therefore involve increased dopamine functioning and accordingly dopamine antagonists are its appropriate treatment.

However, the picture in real life is considerably more ambiguous. In the first place there has long been a substantial amount of evidence that up to a third of individuals with ‘schizophrenia‘ actually do well on psychostimulants. Read more…

Anticholinergics

The anticholinergics are a group of drugs, examples of which are given in the table below, which antagonise the action of the neurotransmitter acetylcholine (Ach) at one of its receptors – the muscarinic receptor.

These drugs were initially used to treat Parkinson’s disease. They have since largely been superseded by the use of L-dopa. As most neuroleptics commonly cause parkinsonian symptoms, the anticholinergics have been used routinely to alleviate side effects, where the effect of L-dopa would be blocked by the neuroleptics themselves.

It has been suggested that they have been used too routinely. In many instances it has been common practice to prescribe an anticholinergic agent along with a neuroleptic, when the neuroleptic is first given – that is even before side effects have appeared. The rationale for this has been that the emergence of side effects may compromise an individual’s willingness to continue with medication. The more cynical view is that an early prescription of an anticholinergic drug means that hospital staff or general practitioner will not be called out of hours by a distressed patient, who has just been paralysed by a dystonic reaction or had some other side effect. This of course ensures that they both get a night’s sleep. Read more…